Adult periodontitis is a chronic inflammatory disease of bacterial etiology that results in alveolar bone loss. It has been reported recently that alveolar bone mass is reduced in women who have adult periodontitis. In addition, individuals with spinal osteoporosis have low mandibular bone mass compared to normal women. Studies in animals and humans have shown that the bisphosphonate, alendronate, can prevent bone loss by inhibiting osteoclast-mediated bone resorption and may also reduce local and systemic levels of inflammatory cytokines and some new bone formation. However, bisphosphonates and other therapies do not return bone mass to normal. However, bisphosphonates and other therapies do not return bone mass to normal. Administration by daily infection of parathyroid hormone (hPTH 1-34) has been found to stimulate new bone formation in patients. The goal of the present study is to restore lost bone in adult patients with severe periodontitis and low mandibular bone mass. The hypothesis underlying this study are: (1) that two years of bisphosphonate administration in conjunction with conventional periodontal therapy will lead to significantly greater new bone formation and gains in clinical attachment and alveolar bone height than conventional therapy alone, and that (2) in patients with bisphosphonate, the addition of hPTH (1-34) treatment, when used in conjunction with conventional periodontal treatment will significantly increase alveolar bone mass and may restore alveolar bone mass toward normal as compared to individuals treated with placebo and bisphosphonate. To test these hypotheses, a two-study will be conducted. In years 1-3, a 2-year randomized, placebo-controlled trial will be performed to determine if conventional periodontal therapy plus bisphosphonate will promote gains in clinical attachment and alveolar bone height in patients with adult periodontitis and low mandibular bone mass. In phase two (years 3-4), the bisphosphonate treatment group will be re-randomized to either hPTH (1-34) or placebo to determine whether addition of hPTH further restores bone mass and clinical attachment levels. Secondary outcomes include determining whether there is an association about specific IL-1 genotype and responsiveness to treatments.